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SARS‐CoV‐2 infection causes pulmonary shunt by vasodilatation
Author(s) -
BritoAzevedo Anderson,
Pinto Eduardo Costa,
Cata Preta Corrêa Gabriel Angelo,
Bouskela Eliete
Publication year - 2021
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.26342
Subject(s) - virology , covid-19 , medicine , shunt (medical) , cardiology , infectious disease (medical specialty) , disease , outbreak
Patients with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) may present a significant hypoxemia. The exactly mechanism of such hypoxemia in patients with coronavirus disease 2019 (COVID‐19) is not well described. It has been suggested that microthrombosis contributes to this mechanism, increasing pulmonary dead space. However, dead spaces would not be sensible to oxygen supplementation, and also, enlargement of pulmonary vessels it has been evidenced. Shunt mechanism by vasodilatation, instead, could explain decubitus dependence in oxygenation by blood redistribution as observed in these patients, and moreover, would be more sensible to oxygen supplementation than dead spaces. We hypothesized that SARS‐CoV‐2 causes an intrapulmonary vascular dilatation (IPVD), determining a shunt mechanism by vasodilatation. We performed contrast‐enhanced transthoracic echocardiography to search IPVD shunt in patients with confirmed COVID‐19, hospitalized in an intensive care unit. Ten patients were recruited; one patient was excluded due to low quality of echocardiographic image, and nine patients were included. IPVD was found in seven (78%) patients, with different grades, including patient with normal compliance and the one without invasive ventilation. We demonstrated that shunt by IPVD is present among patients with COVID‐19, and this mechanism is probably implicated in significant hypoxemia observed.